We will continue to study mechanisms by which the ciliary epithelium, ocular vasculature, and aqueous outflow channels maintain intraocular pressure. The ciliary eipithelium will be studied under conditions of injury and repair to learn about the newly formed epithelia. Endogenous humoral and pharmacologic influences upon the turnover of aqueous inflow will be measured by clearance techniques. Factors governing outflow resistance will be looked for by discovering the presence of enzyme systems for the synthesis and degradation of these substances, e.g. mucopolysaccharides. The mechanism of action of adrenergic drugs on intraocular pressure will be studied. An attempt will be made to isolate adrenergic receptros by pharmacologic, chemical and anatomic techniques. Mediators and mediator pathways associated with ocular irritative response, especially miosis and hyperemia, breakdown of the blood-aqueous barrier and elevated intraocular pressure will be studied.